biological therapies for sz Flashcards

1
Q

there are two types of antipsychotics which are used to treat sz

A

typical and atypical

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1
Q

antipsychotics are dopamine antagonists because they bind to complementary dopamine receptors on the post synaptic membrane , thus preventing dopamine molecules from binding to these sites , the result is an

A

inhibitory effect , where there is a lower rate of action potential generation in the postsynaptic membranes and so returns neurotransmission to a normal level

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2
Q

typical antipsychotics are described as ‘ first generation ‘ because these were the drugs historically prescribed to treat sz patients , the main example of a typical antipsychotic would be chlorpromazine it is

A

particularly favoured in psychiatric institutions due to its calming and sedative effects , due to acting upon histamine receptors in addition to dopamine receptors

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3
Q

atypical antipsychotics are described as ‘ second generation ‘ because they were developed to add to the effectiveness of first generation medications and also

A

alleviate the serious side effects associated with such drugs

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4
Q

atypical antipsychotics work in the same way as typical antipsychotics but also target other neurotransmitter receptors on post synaptic membranes in line with more modern research for example

A

clozapine targets serotonin and glutamate receptors , whilst risperidone acts on dopamine and serotonin receptors

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5
Q

the key advantage of clozapine is the improvements in cognitive functioning and mood which patients experience when taking it , this is particular useful considering that sz has a 50% co morbidity rate with depression however

A

these benefits may be offset by the serious side effect of agranulocyotis which is a severe and dangerous leukopenia which has caused several deaths in the past

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6
Q

on the other hand the key advantage of risperidone is that smaller doses are required because it acts more strongly on dopamine receptors compared to

A

Clozapine, and so would be particularly suited to patients who do not suffer from depression but have a previous history of blood-related illnesses.

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7
Q
  • the development of the antipsychotics was mainly based upon the dopamine hypothesis and so their use depends on this theory too
    for example if antipsychotics appear to alleviate symptoms by reducing the action of dopamine , this makes sense considering the original dopamine hypothesis ie hyperdomapinergia in the sub cortex. however this action is not in line with the revised version of the dopamine hypothesis which suggests that
A

abnormally low levels off dopamine in the cortex are responsible for symptoms.
therefore , a further reduction in dopamine levels should make symptoms worse and not better.
this paradox had caused some to question the validity of the use of antipsychotics as well as the accuracy of the dopamine hypothesis as an explanation for sz.

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8
Q
  • a serious consideration which must be made when using antipsychotics is thinking about the side effects
    the short term side effects of typical antipsychotics are relatively mild ie wright gain and agitation , whilst the long term risk include tardive dyskinesia and neuroleptic malignant syndrome (NMS) characterised by fever , altered mental states , and is thought to be caused by dopamine receptor blockage or central nervous system infections. these side effects are not offset by
A

atypical antipsychotics , where agranulocyotis remains a serious concern for those taking clozapine , whose state must be continually monitored using blood tests.
therefore a cost benefit analysis should be carried out to consider whether the benefit of symptom reduction outweighs the cost of side effects for each specific patient

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9
Q
  • despite there being a rage of evidence supporting the use of typical (thornley et al) and atypical antipsychotics (meltzer) these studies still suffer from problems of validity
    as suggested by Healy. for example since chlorpromazine has particularly powerful sedative effects , then this suggests that studies reviewing the effectiveness of antipsychotics in terms of symptom reduction may actually be measuring how calm and functional the patient appears to be - simply suppressing the symptoms is not a way of controlling them and so such studies may lack
A

validity due to not accurately assessing the actual effectiveness of antipsychotics in treating the proximal cause of sz
secondly drug companies are selective about what type of information they publish : many focus on the short term benefits as opposed to the long term risks and use inapporpiate control groups , such as patients suffering from withdrawal symptoms as they have stopped taking their medication.
this distorted focus brings into question , yet again , the validity of research into the effectiveness of antipsychotics

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